Biomedical subjects
A E Becker
Publications and source records attributed to A E Becker.
The heart after surgery for congenital heart disease.
The pathology of the heart following surgical correction for congenital cardiac defects has not been fully explored. This study is based on valvar aortic stenosis, atrioventricular septal defect, complete transposition of the great arteries, and Fallot's tetralogy. Emphasis has been put on preexistent gross pathology, with histological verification, and postoperative complications. Among patients with aortic valve stenosis preexistent anomalies dominated (left ventricular hypoplasia, mitral valve abnormalities, left ventricular endocardial fibroelastosis). The findings suggest that the cases represent an extreme within a spectrum and could explain the late postoperative dismal results in patients suffering from congenital left heart obstruction. In patients with atrioventricular septal defects the important pathology related predominantly to the operative procedure (injury to the atrioventricular bundle, patch dehiscence at the site of the atrioventricular node, inadequate repair of the left atrioventricular valve leaflets) and to pulmonary obstructive vascular disease. In complete transposition of the great arteries, with or without ventricular septal defects, technical problems dominated. Obstruction of the systemic and pulmonic venous pathways, atrial dysrhythmia, and tricuspid valve injury were the most serious complications following Mustard's procedure. The Rastelli-type procedure was complicated by degeneration and calcification of the porcine valve and crowding of the left ventricle. The arterial switch was complicated by abnormal origin and course of the left circumflex artery, which led to kinking and myocardial infarction. In Fallot's tetralogy surgical complications (injury to the atrioventricular bundle and the tricuspid valve) were the most important. The study discloses that the heart after surgery for congenital heart disease cannot be considered without taking preexistent pathology into account. Careful preoperative investigations are mandatory, since most anomalies could have been detected and, hence, might have changed the operative result.
Surgery for left ventricular outflow tract stenosis in atrioventricular septal defect.
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Comparison of mackerel-oil and lard-fat enriched diets on plasma lipids, cardiac membrane phospholipids, cardiovascular performance, and morphology in young pigs.
Purified mackerel-oil extract or lard fat (9.1% wt/wt) was added to a basal diet of young pigs for 8 wk. Effects on plasma lipids, glucose and insulin, cardiac membrane phospholipids, cardiovascular performance, and morphology were studied. A time-dependent reduction of plasma triglyceride (62%), total cholesterol (41%), and HDL cholesterol (47%) was found in the mackerel-oil-fed pigs. The postprandial glucose and insulin response may indicate a mackerel-oil-induced resistance of insulin receptors. Although the polyunsaturated fatty acid composition of cardiac sarcolemma widely differed between the two groups, all determined indices of heart function were equal. It is concluded that consumption of a fish-oil diet with a low content of monoenes and supplemented with antioxidants reduces plasma lipid levels without producing pathological side effects.
Sudden death in a young competitive athlete with Wolff-Parkinson-White syndrome.
The case history is documented of a young competitive athlete known to have the electrocardiographic pattern of the Wolff-Parkinson-White syndrome, but considered asymptomatic. On that basis competitive sport was not proscribed. In retrospect, he had experienced occasional tachycardias which were of short duration and ended spontaneously. He never requested medical advice. The boy was first admitted for an attack of rapid heart beating which did not readily subside. He was medicated with prajmalium and left the hospital in stable condition. He died suddenly 10 days after discharge. Autopsy examination of the heart revealed an accessory atrioventricular connection in the posterior septal region. The case history underlines that in some patients with the Wolff-Parkinson-White syndrome the clinical manifestation can be minimal and may be easily ignored by the patient. In retrospect, benign episodes of rapid heart beating most likely were due to a circus movement tachycardia, related to an accessory atrioventricular connection. The sudden death can be attributed to atrial fibrillation with rapid ventricular response via the anomalous connection, despite medical treatment. The observation endorses the potential danger of the Wolff-Parkinson-White syndrome in patients with minimal clinical manifestations. A meticulous histologic study of the atrioventricular junction in hearts of young athletes with sudden and unexplained death is a necessity.
Dilated cardiomyopathy: diagnostic accuracy of endomyocardial biopsy.
A histopathological index of contractility failure, which was reported to be accurate for the diagnosis of idiopathic dilated or congestive cardiomyopathy in Japan, was used to assess endomyocardial biopsy specimens from 41 Dutch patients with suspected dilated cardiomyopathy. The calculated index had a sensitivity of 62.5% and a specificity of 68% for idiopathic dilated or congestive cardiomyopathy. These disappointing results indicate that the histopathological index of contractility failure does not reliably distinguish between idiopathic dilated cardiomyopathy and other diseases that cause congestive heart failure.
Pathological changes induced by repeated percutaneous transluminal coronary angioplasty.
The histopathological appearances of seven coronary arteries obtained from four patients after repeated percutaneous transluminal coronary angioplasty were analysed. A complex picture was found; typically there were ruptured atherosclerotic plaques, plaque dissection, and a fibrous tissue response. The histopathological appearance of older and more recent fibrous lesions was different. Older lesions contained more collagen and elastin fibres, whereas recent ones had more loosely arranged connective tissue containing abundant glycosaminoglycan and readily identifiable cells. The fibrous tissues tended to be damaged at the sites of previous injury and where the vessel wall was thinnest. In five of the seven arteries there was evidence of a repeated fibrous response to injury with partial or total rupture of the original media. In one instance a repair response within a pre-existing atherosclerotic plaque had caused restenosis. The results indicate that restenosis after repeated percutaneous transluminal coronary angioplasty, like restenosis after a first procedure, is mainly the result of fibrocellular tissue response to injury of the wall tissues. Because older (that is more mature) repair tissue contains fewer cells and more connective elements than younger repair tissue (that is the loosely arranged connective tissue found soon after angioplasty), when it is disrupted by a further angioplasty procedure it is less capable of producing tissue that will obstruct the lumen. This may explain why in the majority of patients with restenosis repeated percutaneous transluminal coronary angioplasty is successful. The present study also showed that occasionally plaque haemorrhages may become organised and incorporated into the pre-existing atherosclerotic lesion.
Balloon valvuloplasty in congenital and acquired heart disease: morphologic considerations.
Balloon valvuloplasty has already gained its place as an alternative option in the treatment of valvar stenoses. In congenital valvar stenosis its application will be limited because of the complexity of the underlying valve deformities. Nevertheless, isolated pulmonary and aortic valve stenosis are amenable to this form of treatment. The major limitations are undeveloped arterial valve rings and valve dysplasia. In acquired valvar stenosis the main limitation of balloon valvuloplasty seems to be massive calcification of the affected valves. Basically, in both the arterial and atrioventricular position, balloon valvuloplasty splits fused commissures and fractures calcific deposits. Excessive radial pressures may cause tears of the leaflets. The potential of thromboembolic complications, therefore, warrants caution. The nature of the damage inflicted on pathologic valves almost by necessity dictates that restenosis will occur and - most likely - with a high incidence.
[Reappraisal of endomyocardial biopsy with special reference with histopathological contractility failure (HCF) index and histological variability of pick-up specimen obtained from autopsy cases with idiopathic dilated cardiomyopathy].
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Surgical anatomy of left ventricular outflow tract obstruction in complete atrioventricular septal defect. A concept for operative repair.
An integral part of the heart with an atrioventricular septal defect and a Rastelli type A valve configuration is left ventricular outflow tract obstruction. Current surgical techniques do not cater to this particular anatomic facet, and left ventricular outflow tract obstruction has been reported as a postoperative problem. The present study has focused on the surgical anatomy of the mode of attachment of the left superior atrioventricular valve and its relationship to the left ventricular outflow tract. It appeared that the anchoring of the superior leaflet was a major factor in limiting the excursions of the superior leaflet, contributing also to the tightness of the subaortic left ventricular outflow channel. On that basis a surgical repair is proposed in which the greater part of the tightly bound superior leaflet is detached from the septal crest, so that the left ventricular outflow tract is widened.
Multiple aneurysms of the coronary arteries as the cause of sudden death in childhood.
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Description of ventricular septal defects--or how long is a piece of string?
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The coronary arterioles in newborns, infants and children. A morphometric study of normal hearts and hearts with aortic atresia and complete transposition.
The state of development of the intramyocardial coronary arterioles in normal hearts and hearts with congenital malformations is unknown, although these vessels play an important role in regulating myocardial blood flow. To remedy the situation, we studied 64 normal hearts (ranging in age from 23 weeks gestational age to 75 years), 13 hearts with complete transposition (5 with intact ventricular septum and 8 with a defect) and 11 hearts with classical aortic atresia. The medial thickness of arterioles with an external diameter from 20 to 100 microns was measured. The number of arterioles was calculated per mm2; a distinction was made between vessels between 20 and 100 microns and those smaller than 20 microns. The results show that the arteriolar vascular bed is not yet full grown at term. Within the first year of life the medial smooth muscle mass increases, most likely due to growth and peripheral extension onto the smaller branches. In the hearts of patients with aortic atresia who lived for a week or less, the arteriolar media appeared to lag behind that in normal hearts. In those patients who survived into the second post-natal week, however, the arteriolar bed was almost as anticipated for normal. The normal values obtained in the latter group could be due to intrinsic differences, rather than expressing actual and rapid growth.
Double outlet right ventricle: an unusual variant with overriding of both great arteries, absent outlet septum and mitral-to-aortic-to-pulmonary valve continuity.
Double outlet right ventricle constitutes a spectrum of anomalies unified by the fact that both great arteries for their major part arise from the right ventricle. The cases are subcategorized on the basis of the relationship of the great arteries, the precise position of the ventricular septal defect and the muscular morphology of the outflow tracts. The spectrum extends into cases of double outlet left ventricle, while the "in between" cases have been catalogued as double outlet both ventricles. Two hearts are described with overriding of both great arteries, which on morphometric outlet septum and mitral-to-aortic-to-pulmonary valve continuity. To the best of our knowledge, this is the first report of this anatomical arrangement in double outlet right ventricle. Two cases with a similar arrangement have been documented as double outlet left ventricle and double outlet both ventricles. Our two cases further illustrate that the use of the segmental sequential approach to congenital heart disease caters for the most unusual specimens.
Sudden cardiac death and acute pathology of coronary arteries.
The pathology of sudden cardiac death still is a matter of controversy, particularly with respect to the state of the coronary arteries. A recent study has shown a high incidence of acute lesions and suggests a causal relationship. The present study has been designed to verify whether or not acute coronary arterial lesions occur frequently in patients with sudden cardiac death. Sixteen hearts were available. In each instance the patient had died within 6 hours from the onset of myocardial ischaemia. The coronary arterial system was extensively studied by post-mortem coronary angiography, decalcification, serial blocking and histological sectioning. Acute coronary arterial lesions, defined as plaque fissure, 'isolated' plaque haemorrhage and 'isolated thrombosis', were found in 14 of the 16 hearts (87.5%). The total number of acute lesions in the 14 hearts was 28. In 9 hearts plaque fissures were present, in 7 'isolated' plaque haemorrhages and in 5 an 'isolated thrombus'. Half of all acute lesions had occurred in an atherosclerotic plaque of pre-existing 50-75% luminal narrowing. The present study endorses the concept that acute coronary arterial lesions occur in a high proportion of patients with sudden cardiac death, plaque fissures with intramural haemorrhage and intraluminal thrombosis being the most common abnormality. It is tempting to attribute causal significance to such lesions in patients with sudden cardiac death.
Bacterial endocarditis of the aortic valve with septic coronary embolism and myocardial infarction in a 4-month old baby.
A 4-month old baby, who developed infective endocarditis of the aortic valve following purulent arthritis of the hip joint, is presented. The baby developed signs of myocardial infarction and died suddenly at the age of 6 months. Autopsy revealed a localized healed coronary arteritis, almost certainly due to an infected embolus, as the underlying cause.
On a possible role for calcium antagonists in atherosclerosis. A personal view.
An overview is provided of current thinking regarding the origin(s) of atherosclerosis on the basis of clinical evidence, experimental models and pharmacological investigations with calcium antagonists. Because this group of drugs inhibits the influx of Ca2+ into the smooth muscle cell of the cardiovascular wall, it has been argued that when endothelial damage is anticipated or has occurred, the 'protective' action of calcium antagonists might avoid, delay or even help to repair the calcium overload seen with cell membrane damage. In the real world the situation must be far more complex as will become evident but as a concept the avoidance of Ca2+ overloading is enticing. In fact, based on circumstantial evidence, a major clinical trial is currently in progress in which the long term effect of nifedipine on coronary atherosclerosis is being evaluated in a double blind randomized fashion. The end-point of this study lies in the reduction of the severity and number of coronary artery lesions. Although not yet completed, the design and goals of that study are provided.